Figure 3

Summary of the cortical microvascular responses to graded hypercapnia and NMDA assessed with laser-speckle contrast imaging and analysis. (a) Peak increases in CoBF to graded hypercapnia (n = 6) were significantly blunted after NMDA-treatment (n = 7) alone but not after MK-801 + NMDA coapplication (n = 4) or AAAN pretreatment (n = 7). NMDA-induced peak increases in CoBF were also attenuated by MK-801 (F_group = 3.785; η² = 0.066; p = 0.012), but not by AAAN, furthermore AAAN clearly had no effect on the microvascular response to graded hypercapnia. (b) determination of the integrated (area under the curve, AUC) CoBF response shows also the severe attenuation of microvascular reactivity to graded hypercapnia in the NMDA-treated animals. Also, the inhibitory effect of MK-801 on NMDA-induced cortical hyperemia is striking (F_group = 4.464; η² = 0.411; p = 0.0001). (c) Cortical microvascular reactivity to hypercapnia is expressed as the ratio of the total CoBF response to the first and second graded hypercapnia. The response was fully preserved in the control and in the MK-801 + NMDA treated animals, however, virtually abolished in the animals exposed to NMDA alone. Pretreatment with AAAN resulted in a partial preservation of the response (F_group = 8.428; η² = 0.441; p = 0.0001). (d) Relative (%) changes in pial arteriolar diameters show that pial arteriolar responses to graded hypercapnia were not significantly different among the four groups. However, NMDA-induced pial arteriolar vasodilation was fully prevented by MK-801 and also significantly attenuated by AAAN (F_group = 4.741; η² = 0.113; p = 0.004), p < 0.05, * vs. NMDA, † vs. control.